Intracardiac thrombus causing peritoneovenous shunt failure: detection by two-dimensional echocardiography.

Peritoneovenous shunts have become an accepted mode of therapy for ascites refractory to medical treatment. However, their use is known to be associated with significant morbidity and mortality. Reported is the case of a patient with a Denver shunt who developed massive intracardiac thrombosis and subsequent shunt malfunction, despite preserved shunt patency.

Iodine-123 phenylpentadecanoic acid and single photon emission computed tomography in identifying left ventricular regional metabolic abnormalities in patients with coronary heart disease: comparison with thallium-201 myocardial tomography.

Iodine-123 phenylpentadecanoic acid (IPPA) is a synthetic long chain fatty acid with myocardial kinetics similar to palmitate. Two hypotheses were tested in this study. The first hypothesis was that IPPA imaging with single photon emission computed tomography (SPECT) is useful in the identification of patients with coronary artery disease. Fourteen normal volunteers (aged 27 +/- 2 years) and 33 patients (aged 54 +/- 11 years) with stable symptomatic coronary artery disease and at least one major coronary artery with luminal diameter narrowing greater than or equal to 70% were studied with symptom-limited maximal exercise testing. The IPPA (6 to 8 mCi) was injected 1 min before the termination of exercise, and tomographic imaging was performed beginning at 9 min and repeated at 40 min after the injection of IPPA. Nine of the normal volunteers and 13 of the patients had a second examination performed at rest on another day. Using the limits of normal as 2 SD from the normal mean values, 27 of the 33 patients with coronary artery disease demonstrated abnormalities in either the initial distribution or the clearance of IPPA, or both. Nineteen of the 33 patients had a maximal variation of activity distribution of greater than or equal to 25% on the 9 min IPPA images. Twenty-two of the 33 patients had a maximal variation in IPPA washout greater than 17% and 17 had a washout rate less than or equal to 2%. There was good agreement between the location of significant coronary artery stenoses and abnormalities in the initial distribution and clearance of IPPA. The second hypothesis tested was that IPPA imaging is as or more sensitive and, therefore, complementary to thallium-201 imaging in the identification of exercise-induced ischemia in patients. Twenty-five of the 33 patients underwent both thallium-201 and IPPA tomographic imaging after symptom-limited maximal exercise testing. The amount of exercise performed by each patient during both studies was similar. Twenty-one of the 25 patients had abnormal IPPA tomographic studies, whereas 18 had abnormal thallium-201 tomographic studies (p = NS). The results of this study suggest the following conclusions: 1) iodine-123 phenylpentadecanoic acid imaging using single photon emission computed tomography and exercise provides a sensitive and relatively noninvasive method for identifying abnormalities in myocardial metabolism associated with significant coronary artery stenoses, and 2) iodine-123 phenylpentadecanoic acid is at least as sensitive as thallium-201 for this purpose using tomographic imaging and exercise testing.

Abnormal myocardial fatty acid metabolism in dilated cardiomyopathy detected by iodine-123 phenylpentadecanoic acid and tomographic imaging.

The radioidinated synthetic fatty acid iodine-123 phenylpentadecanoic acid (IPPA) has proven useful in the identification of regional abnormalities of cardiac metabolism in patients with myocardial ischemia. The present study was performed to test the hypothesis that the myocardial distribution and turnover of fatty acids, assessed noninvasively with IPPA, are altered in patients with cardiomyopathy. Nine normal volunteers and 19 patients with dilated cardiomyopathy of various etiologies underwent cardiac imaging with single-photon emission computed tomography (SPECT) after intravenous injection of IPPA. Apical short-axis and basal short-axis sections were reconstructed and quantitatively analyzed for relative IPPA activity distribution and washout. Patients with congestive cardiomyopathy demonstrated significantly greater heterogeneity of IPPA uptake than normal subjects (maximal percent variation of activity 27 +/- 11 vs 18 +/- 4, p less than 0.01). They also demonstrated a more rapid percent washout rate than control subjects (24 +/- 8 vs 17 +/- 6 for the apical short-axis section, p less than 0.05; 26 +/- 7 vs 18 +/- 5 for the basal short-axis section, p less than 0.01). These abnormalities of fatty acid distribution and turnover were independent of the etiology of the cardiomyopathy. The degree of heterogeneity of IPPA uptake was significantly related to the patients' New York Heart Association functional class (r = 0.64, p less than 0.01). Thus, compared with normal myocardium, the myocardium of patients with congestive cardiomyopathy demonstrates a more heterogeneous distribution of fatty acid uptake, which parallels the clinical severity of the disease. Furthermore, patients with congestive cardiomyopathy demonstrate a more rapid myocardial clearance of the labeled fatty acid, as assessed with SPECT imaging.

Monoclonal antibodies against human monocytes. II. Recognition of two distinct cell surface molecules.

Three monoclonal antibodies (63D3, 63D2, and 61D3) with reactivity against human monocytes have been studied. They reacted with most adherent mononuclear cells but not with pure populations of peripheral blood B and T lymphocytes. Two of these antibodies, 63D3 and 63D2, competed in fluorescence inhibition experiments, recognized a monocyte surface antigen of about 200,000 daltons, and were idiotypically related. The third antibody, 61D3, did not compete with the others in fluorescence inhibition experiments, recognized a different surface molecule, and was idiotypically distinct from 63D3 and 63D2. Whereas 63D3 and 63D2 reacted very weakly with some granulocytes, 61D3 did not, suggesting that it is specific for monocytes alone.

Detection of alterations in left ventricular fatty acid metabolism in patients with acute myocardial infarction by 15-(p-123I-phenyl)-pentadecanoic acid and tomographic imaging.

15-(p-iodine 123-phenyl)-pentadecanoic acid (IPPA) is a synthetic radiolabeled fatty acid with kinetics similar to palmitate. Fourteen patients who had had an acute myocardial infarction 7 +/- 6 days earlier and 9 normal volunteers were studied after being injected with IPPA. The volunteers were remarkable for homogeneous uptake and metabolism of IPPA; 13 of 14 infarct patients showed areas of decreased uptake > 2 SDs below the mean of the volunteers. Metabolism was homogeneous in the volunteers (14.2% +/- 5.8%) and was significantly higher than in regions identified as infarcted (3.9% +/- 12.1%, p < 0.001). Noninfarcted regions in the patients demonstrated significantly increased rates of IPPA metabolism compared to rates in volunteers (23.0% +/- 9.6% p < 0.001). We conclude that patients with recent myocardial infarction have abnormalities of fatty acid metabolism such as decreased uptake and clearance of fatty acid in regions of infarction and normal uptake but relatively increased fatty acid clearance in unaffected regions of the myocardium.

Pneumococcal endocarditis update: analysis of 10 cases diagnosed between 1974 and 1984.

We analyzed the clinical characteristics of 10 patients with pneumococcal endocarditis hospitalized between 1974 and 1984. Patients with pneumococcal endocarditis were typically middle-aged men. Forty percent were alcoholic. They sought medical attention early in the course of their illness and were given appropriate antibiotics promptly. The aortic valve was involved in seven patients. Five patients developed signs of severe valvular insufficiency, and congestive heart failure was present at the time of admission in four patients. Only three patients were recognized to have endocarditis prior to death or to the occurrence of a major complication of their infection. The total in-hospital mortality rate among these patients was 50%. Thus pneumococcal endocarditis is generally an acute, left-sided endocarditis that is associated with rapid valvular destruction and a high mortality rate. Unfortunately, recent advances in diagnosis and treatment of bacterial endocarditis have not substantially improved the outcome of this devastating infection.

A monoclonal antibody that identifies human peripheral blood monocytes recognizes the accessory- cells required for mitogen-induced T lymphocyte proliferation.

These studies were carried out to evaluate the functional characteristics of the cells identified by a monoclonal anti-human mononuclear phagocyte (M phi) antibody, 63D3. This antibody reacts specifically with all human peripheral blood M phi and not with normal human peripheral blood T or B cells. By using the fluorescence-activated cell sorter, human peripheral blood mononuclear cells (PBM) were sorted into 63D3-positive and 63D3-negative populations. Cell volume analysis indicated that 63D3-negative cells were identical to the non-adherent cells (NAC) in PBM, whereas 63D3-positive cells had a bimodal size distribution comparable to glass-adherent cells (AC). Neither 63D3-negative cells nor NAC were able to proliferate in response to mitogenic stimulation, whereas co-culture with either mitomycin C-treated AC or 63D3-positive cells restored mitogen responsiveness. Thus, the 63D3-positive population contains the relevant accessory cell required for mitogen-induced human lymphocyte proliferation.

Initial characterization of monoclonal antibodies against human monocytes.

Three monoclonal antibodies against human monocytes have been produced by somatic cell fusion. Extensive specificity analysis suggests that these antibodies react with most if not all human peripheral blood monocytes and not with highly purified T or B cells. Initial chemical characterization of the monocyte antigen recognized by two of these antibodies is presented. The molecule is a single polypeptide chain with an apparent molecular weight of 200,000. These reagents should prove useful in the clinical definition of disorders of monocyte differentiation, in studies of monocyte function, and in the elucidation of the genetics and structure of monocyte cell surface antigens.

Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone.

In patients with atherosclerotic coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate decrease in coronary blood flow and myocardial oxygen supply. This study was performed to explore the mechanism of smoking-induced coronary vasoconstriction and, specifically, to determine if smoking causes an alpha-adrenergically mediated increase in coronary artery tone. In 36 chronic smokers with coronary artery disease (27 men and nine women, 50 +/- 9 [mean +/- SD] years old), heart rate-systolic arterial pressure double product and coronary sinus blood flow (by thermodilution) were measured before and during smoking both before and after (1) normal saline (n = 5, control subjects), (2) an alpha-adrenergic-blocking agent, phentolamine, 5 mg (n = 15), (3) a beta-adrenergic-blocking agent, propranolol, 0.1 mg/kg (n = 12), or (4) sodium nitroprusside, 0.4 to 0.8 micrograms/kg/min, given in a dose sufficient to diminish systolic arterial pressure by 15% (n = 4). During the initial smoking period, rate-pressure product increased and coronary sinus blood flow was unchanged by smoking in all groups. After 30 to 75 min, saline, phentolamine, propranolol, or sodium nitroprusside was given, and measurements were repeated. In the control subjects, rate-pressure product and coronary sinus blood flow responded in a similar manner to that observed previously. In those receiving phentolamine, rate-pressure product was unchanged, but coronary sinus blood flow rose substantially with smoking (percent change +2 +/- 15% during the first smoking period [before phentolamine] and +32 +/- 17% during the second smoking period [after phentolamine]; p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Quantification of myocardial injury produced by temporary coronary artery occlusion and reflow with technetium-99m-pyrophosphate.

Previously, technetium-99m-stannous pyrophosphate (99mTc-PPi) has been used to localize and estimate the size of myocardial infarcts in animals after permanent coronary artery occlusion. This study tested the hypothesis that 99mTc-PPi accurately sizes myocardial infarctions produced by temporary coronary artery occlusion and reflow in dogs. Three groups of dogs were studied: group A underwent 3 hr of occlusion followed by 2 hr of reperfusion, with 99mTc-PPi injected 10 min after reflow (n = 10); group B underwent 3 hr of occlusion followed by 2 hr of reperfusion, with 99mTc-PPi injected 90 min after reflow (n = 11); and group C underwent 3 hr of occlusion followed by reflow with 99mTc-PPi injected at 10 min and again at 48 hr after reflow (n = 5). Myocardial slices from group A and B dogs were imaged in vitro. Group C dogs were imaged with single photon-emission computed tomography (SPECT) in vivo, and myocardial slices were imaged in vitro at the conclusion of the study. The extent of myocardial infarction was defined with triphenyltetrazolium chloride (TTC) staining, and coronary blood flow was estimated with radioactive microspheres. In addition, transmural myocardial tissue samples were taken from the center of the myocardial infarction, the lateral portion of the myocardial infarction, the normal myocardium adjacent to the lateral aspect of the infarcts, and from the normal myocardium and counted for 99mTc-PPi activity. A significant correlation was found between infarct size determined by areas of increased 99mTc-PPi uptake and that estimated from TTC staining for both group A (r = .89) and group B animals (r = .98).(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormal I-123 metaiodobenzylguanidine myocardial washout and distribution may reflect myocardial adrenergic derangement in patients with congestive cardiomyopathy.

I-123 metaiodobenzylguanidine (MIBG) is a new radiopharmaceutical with properties that allow the characterization of the sympathetic innervation of several organ systems. In this study, we used MIBG with tomographic imaging to evaluate noninvasively the differences in myocardial sympathetic innervation in 14 healthy volunteers and 16 patients with severe dilated cardiomyopathy (CM). Initial (15-minute) images demonstrated no significant differences in MIBG concentration in the hearts of patients with CM and of healthy volunteers. However, the myocardial retention of MIBG was significantly reduced in the patients with CM. Expressed as the percent washout from 15 to 85 minutes, the patients with CM had a 28 +/- 12% washout rate compared with 6 +/- 8% in the controls (p less than 0.001). A small subset of patients from each group imaged at 4-hour intervals demonstrated even greater disparity in washout rates. In addition, the patients with CM had significantly greater heterogeneity in the MIBG activity distribution within the myocardial images. There was 47 +/- 15% intraimage variability in MIBG distribution in the patients with CM and 22 +/- 9% variation in the controls (p less than 0.001). We conclude from these data that the myocardial distribution and kinetics of MIBG in images obtained from patients with CM differ significantly from those of controls and that the MIBG patterns may be used as a relatively noninvasive means to evaluate the severity of altered adrenergic innervation in the hearts of these patients.